(1) Background: A considerable number of systematic reviews, with substantial heterogeneity regarding their methods and included populations, on the impact of COVID-19 on infected pregnant women and their neonates, has emerged. The aim was to describe the obstetric-perinatal and neonatal outcome of infected pregnant women and their newborns during the COVID-19 pandemic; (2) Methods: Three bibliographical databases were searched (last search: 10 September 2020). Quality assessment was performed using the AMSTAR-2 tool. Primary outcomes included mode of delivery, preterm delivery/labor, premature rupture of membranes (PROM/pPROM) and abortions/miscarriages. Outcomes were mainly presented as ranges. A separate analysis, including only moderate and high-quality systematic reviews, was also conducted. The protocol was registered with PROSPERO (CRD42020214447); (3) Results: Thirty-nine reviews were analyzed. Reported rates, regarding both preterm and term gestations, varied between 52.3 and 95.8% for cesarean sections; 4.2–44.7% for vaginal deliveries; 14.3–63.8% specifically for preterm deliveries and 22.7–32.2% for preterm labor; 5.3–12.7% for PROM and 6.4–16.1% for pPROM. Maternal anxiety for potential fetal infection contributed to abortion decisions, while SARS-CoV-2-related miscarriages could not be excluded. Maternal ICU admission and mechanical ventilation rates were 3–28.5% and 1.4–12%, respectively. Maternal mortality rate was <2%, while stillbirth, neonatal ICU admission and mortality rates were <2.5%, 3.1–76.9% and <3%, respectively. Neonatal PCR positivity rates ranged between 1.6% and 10%. After accounting for quality of studies, ranges of our primary outcomes remained almost unchanged, while among our secondary outcomes, maternal ICU admission (3–10%) and mechanical ventilation rates (1.4–5.5%) were found to be relatively lower; (4) Conclusions: Increased rates of cesarean sections and preterm birth rates were found, with iatrogenic reasons potentially involved. In cases of symptomatic women with confirmed infection, high maternal and neonatal ICU admission rates should raise some concerns. The probability of vertical transmission cannot be excluded. Further original studies on women from all trimesters are warranted.

Previous Gestational Diabetes Mellitus (pGDM) is a common condition and has been associated with future development of Type 2 Diabetes Mellitus (T2DM) and Metabolic Syndrome (MS) in women affected. The pathogenesis and risk factors implicated in the development of these conditions later in the lives of women with pGDM are not as yet fully understood. Research has recently focused on a group of substances produced mainly by adipose tissue called adipokines, this group including, among others, adiponectin, leptin, Retinol-Binding Protein-4 (RBP-4), and resistin. These substances as well as other inflammatory mediators (CRP, IL-6, PAI-1, TNF-α) seem to play an important role in glucose tolerance and insulin sensitivity dysregulation in women with pGDM. We summarize the data available on the role of these molecules.

The article presents an overview of immunological factors and their role in the genesis and development of endometriosis, with emphasis on inflammatory cytokines and growth and adhesion factors. Although retrograde menstruation is a common phenomenon among women of reproductive age, not all women with retrograde menstruation suffer the disease. Development of endometriosis seems to be a complex process, facilitated by several factors, including quantity and quality of endometrial cells in peritoneal fluid (PF), increased inflammatory activity in PF, increased endometrial-peritoneal adhesion and angiogenesis, reduced immune surveillance and clearance of endometrial cells, and increased production of autoantibodies against endometrial cells. Potential biomarkers like cytokines and autoantibodies, upregulated during development of endometriosis, seem useful in the development of a non-surgical diagnostic tool. In this review work, the immune role in endometriosis is examined through the role of immunological factors in the genesis and development of the disease. Furthermore, it could be concluded that, although endometriosis can be treated using hormonal suppression, there is a need today for non-hormonal drugs, probably to modulate immune function, in order to confront the disease and alleviate pain or infertility without inhibition of ovulation.

Gestational diabetes, occurring during the hyperglycemic period of pregnancy in maternal life, is a pathologic state that increases the incidence of complications in both mother and fetus. Offspring thus exposed to an adverse fetal and early postnatal environment may manifest increased susceptibility to a number of chronic diseases later in life. Compelling evidence for the role of epigenetic transmission in these complications has come from comparison of siblings born before and after the development of maternal diabetes, exposure to this intrauterine diabetic environment being shown to cause alterations in fetal growth patterns which predispose these infants to developing overweight and obesity later in life. Diabetes of the offspring is also mainly the consequence of exposure to the diabetic intrauterine environment, in addition to genetic susceptibility. Since obesity and diabetes are known to increase the risk of cardiovascular disease, cardiovascular sequelae in the offspring of diabetic mothers are virtually inevitable. Research data also suggest that exposure to a diabetic intrauterine environment during pregnancy is associated with an increase in dyslipidemia, subclinical vascular inflammation, and endothelial dysfunction processes in the offspring, all of which are linked with development of cardiovascular disease later in life. The main underlying mechanisms involve persistent hyperglycemia hyperinsulinemia and leptin resistance.

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Diabetes mellitus is associated with an elevation in gynecologic cancer risk. Moreover, there are many studies exploring the prognosis of patients with diabetes and gynecological cancer, the outcome and the overall survival in well-regulated patients.

Acute lung injury (ALI) results in high morbidity and mortality among preterm neonates and efforts have therefore been devoted to both antenatal and postnatal prevention of the disease. ALI is the result of an inflammatory response which is triggered by a variety of different mechanisms. It mostly affects the fetal lung and, in particular, causes damage to the integrity of the lung's alveolar-capillary unit while weakening its cellular linings. Chemotactic activity and inflammatory products, such as proinflammatory cytokines TNF-α, IL-1, IL-6, IL-11, VEGF,TGF-α and TGF-β, provoke serious damage to the capillary endothelium and the alveolar epithelium, resulting in hyaline membrane formation and leakage of protein-rich edema fluid into the alveoli. Chorioamnionitis plays a major part in triggering fetal lung inflammation, while mechanical ventilation, the application of which is frequently necessary in preterm neonates, also causes ALI by inducing proinflammatory cytokines. Many different ventilation-strategies have been developed in order to reduce potential lung injury. Furthermore, tissue injury may occur as a result of injurious oxygen by-products (Reactive Oxygen Species, ROS), secondary to hyperoxia. Knowledge of the inflammatory pathways that connect intra-amniotic inflammation and ALI can lead to the formulation of novel interventional procedures. Future research should concentrate on the pathophysiology of ALI in preterm neonates and οn possible pharmaceutical interventions targeting prevention and/or resolution of ALI.

During active labor the fetus maintains oxygen supply to the brain by redistributing blood flow. In cases of hypoxia this is feasible for only 2 min. We note a strong correlation between fetal pulse oximetry, Doppler velocimetry of the MCA and UA, and fetal morbidity.